Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
βPAK CRISPR/Cas9 KO Plasmid (m): sc-422108
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- βPAK CRISPR/Cas9 Knockout (KO) Plasmid (m) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the βPAK genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
βPAK CRISPR/Cas9 KO Plasmid (m) | sc-422108 | 20 µg | $397.00 |
Overview
Pak3 encodes βPAK (p21-activated kinase 3), a serine/threonine kinase activated downstream of the Rho family GTPases RAC1 and CDC42. βPAK coordinates actin cytoskeleton remodeling, neurite outgrowth, and synaptic signaling through pathways that intersect with MAPK/ERK signaling, cell adhesion dynamics, and activity-dependent neuronal plasticity. In mouse, Pak3 function is particularly relevant to studies of nervous system development and circuit function, where altered PAK signaling can impact dendritic spine morphology and synaptic connectivity. Dysregulation of PAK-family signaling has been linked to neurodevelopmental and cognitive phenotypes, supporting its use in mechanistic studies of neuronal signaling and cytoskeletal control.
βPAK CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Pak3 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Pak3 together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.
The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the Pak3 open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish βPAK protein expression.
This CRISPR knockout system enables efficient generation of Pak3-deficient cell models for investigation of βPAK signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Pak3 exon(s) critical for βPAK function
- Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
- GFP reporter for identification of transfected cells
- Pool of plasmids targeting multiple Pak3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by βPAK CRISPR/Cas9 KO Plasmid (m) and βPAK CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Pak3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by βPAK HDR Plasmid (m) and βPAK HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Pak3 homology arms to support homology-directed repair at defined Pak3 target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.